Craig M. Coopersmith, M.D.

Washington University
School of Medicine

Dept. of Pediatrics
Div. Surgery & Anesthesiology
Box 8109
660 S. Euclid Ave.
St. Louis, MO 63110

tel: (314) 362-9342
fax: (314) 362-1602
email: coopersmithc@wustl.edu
web: Personal Weblink

 

 

RESEARCH INTEREST

Our laboratory is interested in the role of altered intestinal function in the development of sepsis. Sepsis is the leading cause of mortality in critically ill patients nationwide. Gut epithelial apoptosis is increased in human autopsy studies and animal models of sepsis. This laboratory has recently compared intestinal apoptosis and survival in a murine model of P. aeruginosa pneumonia-induced sepsis in transgenic mice that overexpress Bcl-2 in the intestinal epithelium. These results indicate that intestinal epithelial apoptosis may play a role in sepsis-related mortality. We have also found that sepsis induces a p53-independent decrease in gut epithelial proliferation. Because alterations in proliferation, cellular division and apoptosis potentially have functional importance in survival from an overwhelming infection, the gut's regenerative capacity and cell cycle may represent novel targets for future sepsis research.

SELECTED PUBLICATIONS

Husain KD, Stromberg PE, Javadi P, Buchman TG, Karl IE, Hotchkiss RS, Coopersmith CM. Bcl-2 inhibits gut epithelial apoptosis induced by acute lung injury in mice but has no effect on survival. Shock. 2003; 20:437-43.

Coopersmith CM, Stromberg PE, Davis CG, Dunne WM, Amiot DM 2nd, Karl IE, Hotchkiss RS, Buchman TG. Sepsis from Pseudomonas aeruginosa pneumonia decreases intestinal proliferation and induces gut epithelial cell cycle arrest. Crit Care Med. 2003; 31: 1630-7.

Coopersmith CM, Stromberg PE, Dunne WM, Davis CG, Amiot DM, Buchman TG, Karl IE, Hotchkiss RS. Inhibition of intestinal epithelial apoptosis and survival in a murine model of pneumonia-induced sepsis. JAMA2002; 287:1716-1721.

Coopersmith CM, Chang KC, Swanson PE, Tinsley KW, Stromberg PE, Buchman TG, Karl IE, Hotchkiss RS. Overexpression of Bcl-2 in the intestinal epithelium increases survival in septic mice. Crit. Care Med. 2002; 30:195-201.

Coopersmith CM, Chang KC, Swanson PE, Tinsley KW, Stromberg PE, Buchman TG, Karl IE, Hotchkiss RS. Overexpression of Bcl-2 in the intestinal epithelium increases survival in septic mice. Critical Care Medicine 30:195-201, 2002.